Eye Review Flashcards
Label the illustration
How should an eye review Hx be structured?
HOPC (unilateral or bilateral eye problem)
PMHx
Past ocular Hx
FHx
SHx
Rx
Allergies
Outline the structure of the eye exam
VISION, PUPILS, PRESSURE
1) Visual acuity + further examinations according to suspected Dx (e.g. pin hole, contrast sensitivity, colour saturation, Ishihara colour vision test, visual fields by confrontation, light saturation)
2) Pupil reactions: direct, consensual, swinging
3) IOP + additional tests (e.g. corneal reflections, EOMs, cover testing, corneal sensation, red reflex)
4) Slit lamp/fundus examination
How is visual acuity measured?
Using a Snellen chart
Patient is positioned at a predetermined distance from the chart (classically 6 metres) in well illuminated room and covers one eye at a time
Try pinhole if VA is 6/9 or worse
NB Leave distance glasses/bifocals/multifocals on for the test but take reading glasses off
How is contrast sensitivity assessed?
Using a Pelli-Robson contrast sensitivity chart
How can colour saturation be tested?
Ask patient to cover one eye (start by covering “bad eye” if you already know which this is) and look at something red
Then ask them to swap eyes and report any change
“If the intensity of the colour in one eye is worth $1, how much is it worth in the other eye?” E.g. 30 cents in this example
How can colour vision/differentiation be assessed?
Using Ishihara colour plates
How can light saturation be tested?
How is the swinging light test performed and how are the findings interpreted? What does it assess for?
Assesses for RAPD
Swing the light between the two eyes; the pupil with the poorer, functioning anterior visual pathway will dilate despite light stimulus
Describe the light reflex pathway
What is the Marcus Gunn pupil?
RAPD
What is the Argyll Robertson pupil?
Pupil constricts on accommodation (when focussed on an object close-up) but NOT to light
Highly specific sign of neurosyphilis, and may also be a sign of diabetic neuropathy
In general, pupils that “accommodate but do not react” are said to show light-near dissociation - i.e., it is the absence of a miotic reaction to light, both direct and consensual, with the preservation of a miotic reaction to near stimulus (accommodation-convergence)
What is the Holmes Adie pupil?
Tonically dilated pupil that does not react to light
Associated with damage to parasympathetic pupillary fibres
How is IOP measured?
By applying pressure to the cornea using a tono-pen or Goldmann applanation tonometry; IOP is inferred from the force required to “flatten” (applanate) the cornea
Topical anaesthetic should be applied to the eye first to reduce discomfort caused by probe making contact with the cornea
What influences IOP? What is its normal range?
Measurement is influenced by corneal thickness (i.e. a thicker cornea will have more resistance and produce a higher IOP reading)
Normal IOP: 6-21mmHg (mean 15mmHg)
How may visual fields be tested?
By confrontation
By automated perimetry (uses a mobile stimulus moved by a perimetry machine; patient indicates whether he sees the light by pushing a button)
Using an Amsler grid (used to detect visual field defects within the centremost region of the visual field)
How are results of visual field testing recorded?
Documentation is from the patient’s point of view
What do positive findings on Amsler grid testing usually indicate?
Macular pathology
What might abnormal EOMs indicates?
Cranial nerve palsy (III, IV, VI)
Muscle entrapment (e.g. in orbital #)
Muscle infiltrate (e.g. thyroid eye disease)
Muscle weakness (i.e Guillain-Barre Miller-Fisher variant)
Gaze centre dysfunction (e.g. horizontal gaze palsy, internuclear opthalmoplegia)
Internuclear opthalmoplegia
Disorder of conjugate lateral gaze in which the affected eye shows impairment of adduction
Caused by injury or dysfunction in the medial longitudinal fasciculus (MLF); in young patients with bilateral INO, multiple sclerosis is often the cause and in older patients with one-sided lesions a stroke is a distinct possibility
Miller Fisher variant of GBS
Rare, acquired nerve disease characterised by abnormal muscle coordination, paralysis of the eye muscles, and absence of the tendon reflexes; like Guillain-Barré syndrome, symptoms may be preceded by a viral illness
Majority of individuals with Miller Fisher syndrome have a unique antibody that characterises the disorder
How is corneal reflection testing (Hirschberg test) performed?
By shining a light in the person’s eyes and observing where the light reflects off the corneas
6 causes of leukocoria
Cataract
Retinoblastoma
Coats’ disease
Retinal detachment
Retinopathy of prematurity
How is the red reflex tested?
The red reflex refers to the reddish-orange reflection of light from the eye’s retina that is observed when using an ophthalmoscope or retinoscope from approximately 30 cm / 1 foot; examination is usually performed in a dimly lit or dark room
How is cover testing performed and how are results interpreted?
Unilateral cover test is performed by having the patient focus on an object then covering the fixating eye and observing the movement of the other eye; if the eye was exotropic, covering the fixating eye will cause an inwards movement, and esotropic if covering the fixating eye will cause an outwards movement
Dominant fixating eye being covered prompts the other eye to take up fixation (see image)
What is the purpose of cover testing?
Used to determine both the type of ocular deviation and measure the amount of deviation; two primary types of ocular deviations are the tropia and the phoria
Tropia is a misalignment of the two eyes when a patient is looking with both eyes uncovered; a phoria (or latent deviation) only appears when binocular viewing is broken and the two eyes are no longer looking at the same object
What is leukocoria?
An abnormal white reflection from the retina of the eye (seen in place of the normal red reflex)
What is Coats’ disease?
Coats’ disease (AKA exudative retinitis or retinal telangiectasis) is a rare congenital, nonhereditary eye disorder, causing full or partial blindness, characterized by abnormal development of blood vessels behind the retina
How should the slit lamp examination be approached?
Examine from superficial to deep structures:
Lids
Tear film
Conjuctiva
Episclera and sclera
Cornea
Anterior chamber
Iris
Pupil
Lens
Fundus examination
Explain how a fundal assessment should be performed
Dark room, comfortable position for the patient
Ask patient to look into the distance (accommodation constricts the pupil)
Use your R eye for the patient’s R eye and your L eye for the patient’s L eye
Hand on the patient’s forehead allows you to stabilise the distance between the patient’s fundus and fundoscope
Using the dial: green numbers (+) shortens the focal length of the fundoscope and red numbers (-) increase
Once you have the retina in focus, try following a blood vessel to the optic disc
Disc is on nasal side of retina
Revise your fundal anatomy!
What do each of these illustrations demonstrate?
How can myopia and hypermetropia be corrected?
What is astigmatism? What is regular vs irregular astigmatism and what are the implications for Mx?
Normal cornea is curved like a sphere
Regular astigmatic cornea has 2 different curves at 90 degrees to each other and is correctable with glasses or contact lenses
Irregular astigmatic cornea has variable degrees of curvature along each axis and is not easily corrected with glasses-
What is the fastest way to detect a refractive error and how does this work?
Pinhole; obscures the light which has been inappropriately focussed onto the retina
What is presbyopia and how is it managed?
Long-sightedness caused by loss of elasticity of the lens of the eye, occurring typically in middle and old age (lens loses its flexibility with age)
Mx: reading glasses/bifocals
Main causes of cataracts
Age-related
Drugs (e.g. steroids)
Trauma (including intra-ocular surgery)
Systemic diseases (e.g. DM, myotonic dystrophy, Wilson’s disease, atopic dermatitis)
Ocular diseases (e.g. uveitis, retinitis pigmentosa)
Sx of cataracts
Gradual decrease in visual acuity and increase in glare Sx over weeks to years
How is cataract surgery performed? What is the success rate?
Patients often admitted as day case
Usually performed under topical or local anaesthesia
Patient must be able to lie flat and still
Approach: phacoemulsification (emulsification and aspiration of the lens) with insertion of intra-ocular lens
Post-op Abx and steroid eye drops prescribed over 4 weeks
Post-op r/vs at 1 day, week and month
Success rates: visual improvement in >95% of operations performed
What is a cataract?
Clouding of the lens in the eye leading to a decrease in vision
Describe the movement of aqueous humor through the anterior chamber
What are the 3 major clinical features of POAG?
Progressive visual field loss
Progressive increase in cup-to-disc ratio of optic disc
Elevated IOP
NB Some people have high IOP but no evidence of glaucoma (ocular HTN), some people have features of glaucoma despite normal IOP (normal tension glaucoma)
How does visual loss progress in glaucoma?
If the L image is a normal optic disc, what is the pathology on the R?
Increased cup to disc ratio seen in glaucoma
What is the aim of medical Mx for POAG?
To lower IOP and slow disease progression by increasing aqueous outflow or decreasing aqueous production
Lowering IOP slows disease progression, even when IOP is already in normal range
Eye drops for POAG; give an example of each
Prostaglandin inhibitors: latanoprost (Xalatan)
Beta blockers: timolol (timoptic)
Alpha agonists: brimonidine (Alphagan)
Miotics: pilocarpine
Carbonic anhydrase inhibitors: brizolamide (Azopt)
Tablets for treatment of POAG
Carbonic anhydrase inhibitors: acetazolamide (Diamox)
Mechanism of action of prostaglandin inhibitors for Mx of POAG
Increase aqueous outflow
Mechanism of action of B blockers for Mx of POAG
Decrease aqueous production
Mechanism of action of alpha agonists for Mx of POAG
Increase aqueous outflow AND decrease production
Mechanism of action of miotics for Mx of POAG
Increase aqueous outflow
Mechanism of action of carbonic anyhydrase inhibitors for Mx of POAG
Decrease aqueous production
Mx of POAG
Medical: eye drops, tablets
Laser: selective laser trabeculoplasty (SLT; this is a good alternative for pts who do not tolerate or comply with daily eye drops)
Surgical: trabeculectomy (creation of an alternative drainage path for aqueous through the formation of a subconjunctival bleb)
Describe the pathophysiology of uveitic glaucoma
Synechiae (“adhesions”) and inflammatory cells effect fluid dynamics within the anterior chamber
Describe the pathophysiology of neovascular glaucoma
Neovascularisation of angle leads to reduced drainage of aqueous humor and increased IOP
Neovascularisation occurs secondary to ischaemia in the eye (e.g. in setting of central retinal vein occlusion, CRVO, or proliferative diabetic retinopathy)
Leads to characteristic “rubeosis iridis” appearance (new blood vessels seen on surface of iris
How is non-proliferative diabetic retinopathy graded? What findings are seen with each grading?
Mild NPDR: microaneurysms
Moderate NDPR: microaneurysms, intra-retinal haemorrhages, hard exudates, cotton wool spots
Severe NPDR (any one feature of the “4-2-1 rule”): intra-retinal haemorrhages in 4 quadrants, OR venous beading in 2 quadrants, OR IRMA (intra-retinal vascular abnormalities) in 1 quadrant)
Very severe NPDR: 2 features from the 4-2-1 rule
How can retinal microaneurysms be better visualised?
Using fluorescain angiography
Features of mild NPDR
Microaneurysms
Features of moderate NPDR
Microaneurysms
Intra-retinal haemorrhages
Hard exudates
Cotton wool spots
Severe NPDR
Any one of:
Intra-retinal haemorrhages in 4 quadrants
Venous beading in 2 quadrants
IRMA in 1 quadrant
NB If 2 features, this is classified as very severe NPDR
What is proliferative diabetic retinopathy?
Advanced form of diabetic eye disease that occurs when blood vessels in the retina disappear and are replaced by new fragile vessels that bleed easily; can result in sudden loss of vision
Distinguish between low- and high-risk PDR
Low: <1/3 of disc neovascularised (NVD)
High: NVD plus vitreous haemorrhage, OR NVD >1/3 of disc, OR NVE (neovascularisation everywhere!)
How is PDR managed?
Pan-retinal photocoagulation; burns away areas of peripheral retina, decreases drive of VEGF production (leading to reduced neovascularisation), with sacrifice of peripheral vision
What processes can cause diavetic maculopathy?
Macular oedema
Macular ischaemia
Mechanism of macular oedema in diabetic maculopathy
Leakage of fluid into foveal tissue
Lipid exudates adjacent to fovea
Mechanism of macular ischaemia in diabetic maculopathy
Capillary non-perfusion at fovea
What sign on fluorescein angiography indicates macular ischaemia?
Enlarged foveal avascular zone and capillary drop-out
How can macular oedema be visualised?
Using optical coherence tomography (OCT), a non-invasive imaging test that uses light waves to take cross-section pictures of your retina, the light-sensitive tissue lining the back of the eye
Shows fluid leakage and lipid exudates adjacent to fovea
Mx of diabetic macular oedema
Macular (grid) laser
Intra-vitreal anti-VEGF agents
Mx of macular ischaemia
No specific treatment: BSL control, BP control, cholesterol control
What is the most common cause of blindness in people >50 in the developed world?
Dry age-related macular degeneration
Major risk factors for dry macular degeneration
Increasing age
Smoking
Mx for dry macular degeneration
Amsler grid: frequent use allows patient to detect changes/new distortion of vision
Cessation of smoking
Low vision aids
Appearance of dry macular degeneration on fundoscopy and OCT
What is drusen?
What is geographic atrophy?
Drusen are yellow lipid deposits under the retina; while drusen likely do not cause age-related macular degeneration (AMD), their presence increases a person’s risk of developing AMD
Geographic atrophy is the advanced (late) form of dry AMD; atrophy refers to the degeneration of the deepest cells of the retina (retinal pigment epithelium; RPE), which normally helps maintain the photoreceptor cells
What is the classic feature of wet (neovascular) age-related macular degeneration?
Choroidal neovascularisation (CNV): abnormal new vessels grow from choroid to RPE (process linked to increased VEGF levels), and these vessels bleed/leak, leading to macular scarring
Mx of wet macular degeneration
Anti-VEGF agents via (typically monthly) intra-ocular injection: ranbizumab, bevacizumab
Photodynamic therapy
Macular laser
Photodynamic therapy (PDT)
Photodynamic therapy (PDT) is a treatment that uses a drug, called a photosensitizer or photosensitizing agent, and a particular type of light; when photosensitizers are exposed to a specific wavelength of light, they produce a form of oxygen that kills nearby cells
What is the classical appearance of a 3rd nerve palsy?
“Down and out”
What are the major causes of CN III palsy?
Compressive: from tumour, haemorrhage or aneurysm (commonly pupil involving)
Vascular: HTN, DM (commonly pupil sparing)
Trauma
Vasculitis (i.e. GCA)
Demyelinating disease
Idiopathic
Ix of CN III palsy
MRI/MRA urgently if compressive lesion suspected
BP and blood tests for vascular risk factors (including glucose, lipid profile)
Mx and prognosis of CN III palsy
According to the cause
Prognosis is variable
Classic appearance of a CN IV palsy
Tip, turn and tilt
Causes of CN IV palsy
Trauma (can cause bilateral CN IV involvement)
Microvascular disease
Tumour
Demyelination
Vasculitis (GCA)
Idiopathic
Can be congenital
Ix for CN IV palsy
Old photos (if congenital palsy suspected)
Bloods for vascular risk factors
Consider neuro-imaging
Mx of CN IV palsy
According to cause
Prisms in glasses +/- strabismus surgery to re-align the visual axis if not improving
Strabismus
Abnormal alignment of the eyes
What kind of difficulties are experienced by the patient with CN IV palsy and why?
SO allows eye to look down, inwards and provides intortion
A CN IV palsy can cause difficulty reading and walking down stairs
Classic appearance of a CN VI palsy
Abduction deficit
What Sx will a patient complain of with a CN VI palsy?
Horizontal diplopia (binocular)
Causes of CN VI palsy
Vascular
Raised ICP
Tumours
Trauma
Demyelinating disease
Vasculitis (GCA)
Idiopathic
DDx for underlying cause in CN VI palsy
Thyroid eye disease
Medial wall blow-out #
Myaesthenia gravis
Ix of CN VI palsy
Assess vascular RFs
MRI if other associated pathology present, if palsy does not resolve in 3/12 or if patient <40
Mx of CN VI palsy
According to cause
Prisms +/- strabismus surgery
Botox to ipsilateral MR
Interpretation of visual fields
